4.4 Article

Resveratrol suppresses the inflammatory responses of human gingival epithelial cells in a SIRT1 independent manner

Journal

JOURNAL OF PERIODONTAL RESEARCH
Volume 50, Issue 5, Pages 586-593

Publisher

WILEY
DOI: 10.1111/jre.12238

Keywords

anti-inflammatory effect; human gingival epithelial cell; resveratrol; SIRT1

Funding

  1. JSPS KAKENHI [25463215]
  2. Grants-in-Aid for Scientific Research [25463215, 25463216] Funding Source: KAKEN

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Background and ObjectiveIn periodontitis, chronic infection by periodontopathic bacteria induces uncontrolled inflammation, which leads to periodontal tissue destruction. Human gingival epithelial cells (HGECs) constitute a critical first line of defense against periodontopathic bacteria, both as a physical barrier and as regulators of inflammation. Resveratrol, a polyphenol found in grapes and red wine, reportedly has anti-inflammatory properties. Therefore, we investigated the effects of resveratrol on the Porphyromonas gingivalis-induced inflammatory responses of HGECs and their mechanism. Material and MethodsWe stimulated the HGEC line, epi 4, with live or heat-killed P.gingivalis in the presence of resveratrol, and analyzed expressions of the interleukin-8, monocyte chemoattractant protein-1 and interleukin-1 genes. We determined the involvement of SIRT1 in the effect of resveratrol using sirtinol (a SIRT1 inhibitor) or SIRT1 knockdown. We also examined whether the effects were mediated by activation of AMP-activated kinase, suppression of reactive oxygen species, or inhibition of nuclear factor-B (NF-B). ResultsResveratrol treatment decreased the expression of inflammatory cytokines and slightly increased the expression of SIRT1. However, neither SIRT1 inhibition nor SIRT1 knockdown counteracted its anti-inflammatory effects. Although resveratrol did not affect AMP-activated kinase activation or reactive oxygen species production, it slightly suppressed NF-B translocation when cells were stimulated with heat-killed P.gingivalis. ConclusionResveratrol suppressed the inflammatory responses of P.gingivalis-stimulated HGECs, probably by inhibiting NF-B signaling but independent of SIRT1.

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